Both microvascular damage and myocardial cell injury occur after coronary occlusion, but the relationship of these two events is unclear; specifically, it is unknown whether microvascular damage causes myocardial cell injury. Dogs were subjected to coronary occlusion for 20, 40, 60, 90 or 180 minutes, after which subendocardial and subepicardial biopsies were obtained for electron and light microscopy of 1-mu sections. Of 312 biopsies of ischemic myocadium, 181 showed myocardial cell injury with no microvascular damage; 131 showed myocardial cell injury and microvascular damage; but none showed microvascular damage without myocardial cell injury. Although ultrastructural evidence of myocardial cell damage was present in the subendocardium after 20-40 minutes of ischemia, ultrastructural evidence of microvascular damage was not prominent until 60-90 minutes after coronary artery occlusion. Morphologic ultrastructural evidence of microvascular damage lagged behind myocardial cell injury, suggesting that ultrastructural microvascular damage is not a primary cause of ultrastructural myocardial cell injury.

There has been recent interest in treating acute myocardial infarction with coronary reperfusion by fibrinolytic therapy. Experimental studies have shown that myocardial infarct size can be reduced by coronary reperfusion. However, return of cardiac function, high energy phosphate metabolism, and cardiac ultrastructure may be delayed within tissue which is salvaged by coronary reperfusion. This postischemic ventricular dysfunction is transient and has been termed the ‘stunned myocardium’ phenomenon. Although reperfused infarcts are hemorrhagic, the hemorrhage is confined well within tissue which is already necrotic and does not appear to exacerbate the extent of necrosis. Clinical trials designed to assess the benefits of reperfusion for the therapy of acute myocardial infarction should concentrate on long-term rather than short-term changes in cardiac function.

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